A Composite Nuclear Export Signal in the TBP-associated Factor TAF II105

Abstract

TAFII105 is a sub-stoichiometric subunit of TFIID important for activation of anti-apoptotic genes and B cell specific genes by the transcription factors NF-κB and OCA-B. This subunit is highly enriched in B and T lymphocytes, and its expression is regulated at a posttranscriptional level. In the present study we investigated the subcellular localization of TAFII105. In normal B cells, a significant portion of native TAF II105 protein is found in the cytoplasm. Treatment of these cells with B cell-specific stimuli decreased the level of cytoplasmic TAF II105. In adherent cultured cells, TAFII105 is predominantly nuclear; however, a small fraction of the cells showed either cytoplasmic or homogenous distribution of TAFII105. Analysis of different TAFII105 mutants and green fluorescence protein fusion proteins identified a region composed of two adjacent sequences displaying nuclear export activity, suggesting that nuclear export of TAFII105 is mediated by a composite nuclear export signal. TAFII105 nuclear export signal is leptomycin B-resistant indicating that it belongs to a CRM1-independent nuclear export pathway. These results reveal a novel mode of regulation of a specialized component of the general transcription apparatus that may affect the transcription of its target genes.